Biomedical subjects
Publications and source records attributed to R Vijayaraghavan.
A patient with sarcoidosis presented with hoarseness caused by mediastinal lymph nodes compressing the left recurrent laryngeal nerve. The response to corticosteroids was dramatic and complete.
Diisopropyl fluorophosphate (DFP) given to rats in lethal concentration (100 mg/m3, by inhalation for 40 min) significantly inhibited acetylcholinesterase activity in the blood, lung, liver and brain, and induced hyperglycaemia and glycogen mobilization in the liver, diaphragm and brain. Pretreatment (maximum sign-free dose) with carbamates, pyridostigmine (0.075 mg/kg, i.m.) or physostigmine (0.1 mg/kg, i.m.) 15 min before exposure to DFP, modified the inhibited acetylcholinesterase activity only in peripheral tissues. However, the hyperglycaemia and glycogen depletion induced by DFP inhalation were not modified by carbamate pretreatment. The time of survival of DFP exposed animals increased after pretreatment with carbamates, more after physostigmine (81 min) than after pyridostigmine (59 min). The animals exposed to DFP exhibited severe tremors and convulsions as compared to the animals pretreated with carbamates.
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Methyl isocyanate (MIC) either inhaled (5, 10 mg/lit) or administered by intravenous (5, 10, 28 mg/kg) or subcutaneous (1300, 1500 mg/kg) routes produced a dose dependent fall in blood pressure (BP) and heart rate (HR) in anaesthetised rats. Higher doses (10 mg/lit inhalation, 10 & 28 mg/kg i.v., 1500 mg/kg s.c.) increased the lung body weight index (LBI) and tracheobronchial resistance (TBR) concomitant with gross pulmonary damage and edema. However, lower doses (5 mg/lit inhalation, 5 mg/kg i.v., 1300 mg/kg s.c.) produced the cardiovascular depressant effect without affecting LBI, lung morphology and TBR. The effects of MIC on BP, HR and TBR were not counteracted by muscarinic, histaminic and 5-HT receptor blockers and by vagotomy. Studies with hydrolysis products of MIC showed that relatively large doses of methylamine (MA) and dimethylurea (DMU) (i.v.) produced cardiovascular depressant effects, without affecting the LBI & TBR. The results indicate that the cardiovascular depressant effect of MIC may not be entirely a sequel to its effect on respiratory organs, release of vasoactive substances or its hydrolysis products. A non-specific cardiovascular depressant effect of MIC is suggested.
Mice exposed to methyl isocyanate (MIC; 134 mg.m-3 for 30 min = 4020 mg.min-1.m-3) showed a marked loss of body weight after 24 hr and the mean body weight of the exposed group was significantly less than the control, even 15 days after the exposure. No significant change was observed on relative testicular weight. Spermatozoa in the seminiferous tubules disappeared 3 days post exposure. Primary and secondary spermatocytes were hypertrophied. Normalization occurred after 15 days.
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Carbamylation of the N-terminal valine of haemoglobin with methyl isocyanate in rats and rabbits has been demonstrated in vitro and in vivo by gas chromatography. N-Methylcarbamylated haemoglobin, converted by cyclization into 3-methyl-5-isopropylhydantoin, has been quantified by gas chromatography. Standard hydantoin was synthesized, chemically characterized and used for calibration. The method is simple and reliable in the concentration range 0.06-2 nmol. Carbamylation of haemoglobin by methyl isocyanate in vivo in rats can be identified only above a dose of 1.05 mg/l in inhalation exposures. It is inferred that methyl isocyanate in the "active" form crosses the alveolar and erythrocyte membranes and carbamylates the haemoglobin.
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